Epstein-Barr Virus infection results in growth transformation of human B lymphocytes. Despite the persistence of the complete virus genome in infected cells there is usually no virus replication and the infection is said to be latent. However, at least four EBV genes are expressed in "latently" infected growth transformed lymphocytes. The genes and gene products have been largely defined. One of these genes encodes a membrane protein (LMP). LMP appears to aggregate in patches in the plasma membrane. The LMP gene causes rodent cells to partially resist the growth inhibiting effects of medium containing low serum. In Rat-1, but not in 3T3 cells, expression of the gene results in loss of contact inhibition, anchorage independence and enhanced tumorigenicity. Our objectives are to further define (1) the role of the LMP gene in growth transformation, (2) the intracellular location, associations and mechanisms of action of LMP and (3) its relationship to LYDMA, an antigen(s) expressed on the surface of EBV infected cells which is recognized by EBV immune human T cells in their suppression or killing of EBV infected cells.